Researchers discover new protein that plays a key role in insulin resistance and type 2 diabetes

In a finding that could have important implications for the treatment of type 2 diabetes, a team of researchers has discovered a protein that plays a key role in the ability of cells to absorb glucose from the bloodstream.

The findings could lead to an improved understanding of the mechanisms that underlie the development of type 2 diabetes. Currently, it is known that obesity starts a process that eventually causes tissue to become resistant to the effects of insulin, resulting in persistently high blood sugar levels. However, the molecular process that underlies this effect is less clear.

The findings suggest that a deficiency of a protein known as CDP138 may play an important role in why some people who are obese become resistant to the effects of insulin and eventually develop type 2 diabetes.

When blood sugar levels rise, the pancreas releases insulin. This hormone, in turn prompts muscle and fat cells to move a molecule known as GLUT4 from the center of the cell to the surface. This protein actively pulls glucose from the bloodstream into the center of the cell.

Investigators from the Stanford-Burnham Medical Center reported in the journal Cell Metabolism that the protein CDP138 is responsible for pushing GLUT4 from the middle of a cell to its surface. Without CDP138 cells are incapable of absorbing sugar from the bloodstream.

In testing on mice, the researchers found that animals bred to be obese had significantly lower levels of CDp138 than normal mice. Together, these findings indicate that the protein may be an important missing link in the progression from obesity to insulin resistance and type 2 diabetes.

"This is a newly identified protein that's involved in an important step in glucose uptake," said lead researcher Dr Zhen Jiang, PhD.

There is no question of the link between obesity and type 2 diabetes. However, researchers have been unable to completely nail down the mechanism that causes insulin resistance. Some theories have postulated that obesity causes tissue to become inflamed, which damages it and reduces its sensitivity to insulin. Others have proposed that excess fat causes changes to the composition of liver proteins.

However, none of these hypotheses has been able to provide a complete picture of how the body progresses from obesity to insulin resistance and type 2 diabetes. The new findings could provide an important molecular explanation of the phenomenon.

This could enable researchers in the future to develop medications that prevent obesity from causing diabetes. Several groups of researchers have tried to engineer these drugs in the past, with varying degrees of success. However, it is unlikely that a pharmaceutical could be created when researchers do not completely understand the biology that underlies a condition.

While there is still a significant amount of further investigation needed before new drugs could hit the market, the new findings are certainly a step in the direction of more completely understanding how obesity affects type 2 diabetes risk.